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The Voltage-dependent L-type calcium channel subunit alpha-1C, commonly known as CaV1.2, is the primary pore-forming component of the L-type voltage-gated calcium channel complex. It mediates the influx of calcium ions into cells upon membrane depolarization, a process essential for excitation-contraction coupling in cardiac and smooth muscle, as well as neurotransmitter release and gene expression in the central nervous system [1, 10, 16]. In the heart, CaV1.2 is critical for maintaining the plateau phase of the action potential and triggering the release of calcium from the sarcoplasmic reticulum to initiate contraction [11, 20]. Clinically, CaV1.2 is a major therapeutic target for calcium channel blockers (CCBs) such as amlodipine and verapamil, which are widely used to treat hypertension, angina, and certain arrhythmias [12, 15]. Mutations in the CACNA1C gene, which encodes this subunit, are linked to severe conditions including Timothy syndrome, characterized by multi-system defects and long QT syndrome, as well as various neuropsychiatric disorders like bipolar disorder and schizophrenia [10, 14]. Safety concerns associated with targeting this channel include the risk of excessive hypotension, bradycardia, and peripheral edema, necessitating careful dosing and patient monitoring [12, 17].
Calcium channel blocker (antagonist)
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